We will investigate the role of activin signaling in controlling pituitary gonadotrope gene expression and physiology in vivo in transgenic mice. Specific Aim 1 Investigate kinase-deficient type II, IIB, and IB receptors for their activity in blocking activin action in alphaT3-1 cells to further understand the role of activin in the gonadotrope and to choose the optimal dominant negative receptor for creating transgenic mice. Specific Aim 2 Create and characterize transgenic mice in which the activin signaling mechanisms have been disrupted in the gonadotrope. Specific Aim 3 Determine the role of activin signaling in the gonadotrope in vivo utilizing transgenic mice in which pituitary activin signaling mechanisms have been specifically disrupted. The results of these studies will lead to a more thorough understanding of the molecular mechanisms involved in regulating reproductive function.